TIAs (vertebrobasilar)

Jorge Moncayo-Gaete MD (Dr. Moncayo-Gaete of the International University of Ecuador has no relevant financial relationships to disclose.)
Julien Bogousslavsky MD (Dr. Bogousslavsky of the Swiss Medical Network has no relevant financial relationships to disclose.)
Steven R Levine MD, editor. (Dr. Levine of the SUNY Health Science Center at Brooklyn has received honorariums from Genentech for service on a scientific advisory committee and a research grant from Genentech as a principal investigator.)
Originally released December 19, 1994; last updated November 22, 2016; expires November 22, 2019

This article includes discussion of TIAs (vertebrobasilar), vertebrobasilar TIA, and transient ischemic attacks: vertebrobasilar. The foregoing terms may include synonyms, similar disorders, variations in usage, and abbreviations.

Overview

Transient ischemic attacks (TIAs) in the vertebrobasilar arterial system comprise one fourth of all transient ischemic attacks. Their diagnosis is more difficult than that of ischemic attacks in the anterior circulation and often poses a considerable challenge, even for experts. Moreover, vertebrobasilar transient ischemic attacks carry a higher risk of acute stroke than carotid territory TIAs. Timely recognition of the complex symptoms of vertebrobasilar TIAs offers an opportunity to perform an urgent, comprehensive workup and commence treatment that can forestall the onset of permanently disabling neurologic deficit.

In this article, the authors cover the main epidemiological, clinical, pathophysiological, and etiological topics of vertebrobasilar TIAs and comprehensively review the latest assessment tools that identify patients who are at risk of impending post-TIA stroke. The authors also note the most recent and relevant information concerning diagnosis, prognosis, and the therapeutic strategies available for patients suffering a transient ischemic attack in the posterior circulation.

A special section is dedicated to covering the most notable clinical, diagnostic, and therapeutic facets of a peculiar hemodynamic phenomenon, the subclavian steal syndrome, which may occasionally be responsible for transient ischemia in the posterior circulation.

Key points

 

• A posterior circulation infarct may be preceded by a transient ischemic attack in one fourth of patients.

 

• Clinical scores, particularly clinical-plus scores, can help to stratify people who face the highest short-term risk of stroke following transient ischemic attack and can also ensure rapid evaluation and management.

 

• Brain MRI with diffusion-weighted sequences is the preferred diagnostic neuroimaging method within 24 hours of symptom onset. Subsequently, noninvasive evaluation of vertebral and basilar arteries and heart disease should be done.

 

• Prompt secondary stroke prevention is warranted after a transient ischemic attack and should be tailored based on risk factors, etiology, and local circumstances.

 

• Subclavian steal syndrome is often asymptomatic. Neurologic, upper extremity, and – though only very occasionally – coronary symptoms may arise when compensatory mechanisms fail.

 

• Transient ischemic attacks and, more rarely, infarcts in the posterior circulation may be due to subclavian steal syndrome.

 

• Sonography is the initial imaging examination when subclavian steal syndrome is suspected.

 

• Therapeutic interventions, mainly by endovascular approach, are reserved for highly symptomatic patients.

Historical note and terminology

The first clinical description of transient ischemic attack is attributed to Thomas Willis in 1679. In 1911, Marburg described several brainstem syndromes. In 1932, Pines and Gilinsky published clinical details on a patient with a basilar territory infarction. Kubik and Adams later described postmortem material on 18 patients after basilar artery occlusion (Mohr and Caplan 2004). It was not until 1951 that Fisher used the phrase "brief transient attacks of paralysis" in his description of 7 patients with internal carotid occlusion and transient symptoms (Mohr and Caplan 2004). In a separate publication from the same year, Fisher linked occlusive disease at the carotid bifurcation to "transient episodes of blindness, aphasia, paresthesia and paralysis, transient attacks, premonitory fleeting . . . and transient hemiplegia" (Mohr and Caplan 2004). The term "vertebrobasilar insufficiency" arose later from the works of Denny-Brown and Millikan and Siekert in the 1950s (Mohr and Caplan 2004). Currently, the term “vertebrobasilar transient ischemic attack” is preferred to those previously mentioned.

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